Results 51 to 60 of about 60,957 (246)

JAK2 inhibitor persistence in MPN: uncovering a central role of ERK activation

open access: yesBlood Cancer Journal, 2022
The Philadelphia chromosome negative myeloproliferative neoplasms, including polycythemia vera, essential thrombocytosis, and myelofibrosis, are driven by hyper activation of the JAK2 tyrosine kinase, the result of mutations in three MPN driving genes ...
Garima Pandey   +2 more
doaj   +1 more source

Endogenous Ceramide 24:1 Constrains Th17‐Driven Neutrophilic Inflammation by Antagonizing EP2 Signaling

open access: yesAdvanced Science, EarlyView.
Cer24:1 levels are reduced in neutrophilic asthma and inversely correlate with disease severity and airway neutrophilia. Restoring Cer24:1 suppresses pathogenic Th17 differentiation by engaging EP2 on CD4+ T cells, thereby dampening the JAK2–STAT3–RORγt axis and reducing IL‐17 production.
Huan Liu   +11 more
wiley   +1 more source

The genetic and symptomatic link of polycythemia vera. narrative review

open access: yesRevista Mexicana de Investigación Médica
Myeloproliferative neoplasms (MPNs), such as essential thrombocythemia (ET), primary myelofibrosis (PMF), and polycythemia vera (PV), are clonal hematologic disorders.
Asheley Jezabel Flores Hernández   +3 more
doaj   +1 more source

Preclinical studies of Flonoltinib Maleate, a novel JAK2/FLT3 inhibitor, in treatment of JAK2 V617F-induced myeloproliferative neoplasms

open access: yesBlood Cancer Journal, 2022
Janus kinase 2 (JAK2) hyperactivation by JAK2 V617F mutation leads to myeloproliferative neoplasms (MPNs) and targeting JAK2 could serve as a promising therapeutic strategy for MPNs.
Mengshi Hu   +15 more
doaj   +1 more source

Management of MPN beyond JAK2 [PDF]

open access: yesHematology, 2014
Abstract Thrombocytosis has a large number of potential underlying causes, but the dominant group of hematological conditions for consideration in this setting are the myeloproliferative neoplasms (MPNs). In this chapter, we consider several key linked questions relating to the management of thrombocytosis in MPNs and discuss several ...
Claire N, Harrison   +1 more
openaire   +2 more sources

Extracellular Vesicles in Autoimmune Diseases: From Diagnostic Biomarkers to Engineered Therapeutics

open access: yesAdvanced Science, EarlyView.
This review provides a systematic comparison of extracellular vesicles (EVs) from both mammalian and plant sources in the context of autoimmune diseases. It highlights their emerging roles as precision biomarkers and engineered therapeutic platforms.
Yufei Wu   +6 more
wiley   +1 more source

Changes in the cytokine response in the hypothlamus of animals under the influence of chronic social stress: RNAseq data

open access: yesМедицинская иммунология
It is known that chronic social stress leads to immunity disorders in humans and experimental animals. It has been shown that the effect of stress is also manifested in changes in the level of expression of genes involved in the functioning of various ...
A. G. Galyamina   +3 more
doaj   +1 more source

JAK2 V617F down-modulates MPL [PDF]

open access: yesBlood, 2012
Decreased expression of the thrombopoietin receptor (TPOR or MPL) on the cell surface of platelets and megakaryocytes is an established feature of and myelofibrosis; however, the exact mechanism responsible for this phenomenon has gone largely unexplained.
Angela G, Fleischman, Jeffrey W, Tyner
openaire   +2 more sources

SATB2 Mediates H3K9 Delactylation by Recruiting HDAC3 to Repress LCN2 and Inhibit Lung Tumor Growth and Metastasis

open access: yesAdvanced Science, EarlyView.
This study highlights the capacity for tumor suppressor SATB2 to recruit HDAC3 and catalyze histone H3K9 delactylation, thereby repress transcription of the oncogene LCN2. This novel epigenetic‐metabolic axis inhibits the growth and metastasis of non‐small cell lung cancer, delineating a new mechanistic pathway with potential therapeutic relevance ...
Ting Wen   +10 more
wiley   +1 more source

“Intrapericardial Approach” for Venous Outflow Reconstruction in Living‐Donor Liver Transplantation for Budd‐Chiari Syndrome: Surgical Techniques and LongTerm Outcomes

open access: yesAnnals of Gastroenterological Surgery, EarlyView.
Unlike deceased‐donor liver transplantation, living‐donor liver transplantation (LDLT) for Budd‐Chiari Syndrome (BCS) presents distinctive challenges in hepatic venous (HV)‐outflow reconstruction because diseased HV–inferior vena cava (IVC) cannot be entirely replaced with healthy donor vessels.
Koichiro Hata   +4 more
wiley   +1 more source

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